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Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury [ChIP-seq]

ABSTRACT: We profiled Wt1, a key transcription factor, in purified murine podocytes based on ChIP-seq during the time course of podocyte injury by ADR.

ORGANISM(S): Mus musculus

PROVIDER: GSE149486 | GEO | 2020/08/04

REPOSITORIES: GEO

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Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury [RNA-seq]

Project description:We profiled total-RNA data in isolated murine podocytes during the time course of podocyte injury by ADR.

2020-08-04 | GSE154955 | GEO

FOXC2 and WT1 regulate transcriptional reprogramming during the podocyte response to injury

Project description:In the context of human disease, the mechanisms whereby transcription factors reprogram gene expression in reparative responses to injury are not well understood. We have studied the mechanisms of transcriptional reprogramming in disease using murine kidney podocytes as a model for tissue injury. Podocytes are a crucial component of glomeruli, the filtration units of each nephron. Podocyte injury is the initial event in many processes that lead to End Stage Kidney Disease. FOXC2 is a transcription factor known to regulate gene expression in podocytes. FOXC2 and WT1 are both required for podocyte differentiation. Using murine models and human kidney organoids, we investigated FOXC2-mediated transcriptional reprogramming during the course of podocyte injury. Correlating FOXC2 and WT1 ChIP-seq analyses demonstrated that they co-bind many genes expressed in podocytes. Reprogramming the transcriptome involved highly dynamic changes in the binding of FOXC2 and WT1 to target genes during a reparative injury response.

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Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury

Project description:Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury

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Genome-wide analysis of WT1-controlled gene expression in podocytes

Project description:We identified binding sites of the Wilms' tumor suppressor protein WT1 in the mouse podocyte genome in vivo by ChIP-seq. Furthermore, we provide a podocyte transcriptome derived from primary podocytes that were isolated by FACS on mouse glomeruli. In short, we show that WT1 activates a highly specific podocyte transcriptome by binding to putative podocyte-specific enhancers and TSS of target genes. Genes bound by WT1 in podocytes include the majority of genes mutated in hereditary podocytopathies as well as components of the slit diaphragm, actin cytoskeleton, extracellular matrix, and within endocytosis pathways. Furthermore, we infer a podocyte TF network from DNA-binding motifs enriched at WT1-bound loci that includes Tead, Lmx1b, Mafb, Tcf21, and Fox-class transcription factors. Examination of transcription factor binding sites for WT1 by ChIP-seq. Transcriptome analysis of podocytes by RNA-seq.

2014-12-11 | E-GEOD-64063 | biostudies-arrayexpress

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Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury [ChIP-seq]

Project description:Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury [ChIP-seq]

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Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury [RNA-seq]

Project description:Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury [RNA-seq]

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Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-08-04 | GSE154956 | GEO

Podocyte injury in Fabry nephropathy

Project description:Current therapies for Fabry disease are based on reversing intra-cellular accumulation of globotriaosylceramide (Gb3) by enzyme replacement (ERT) or chaperone mediated stabilization, thereby alleviating lysosome dysfunction. However, the therapeutic effect in the regression of end-organ damage (ie. kidney damage) is limited. Ultrastructural analysis of serial human kidney biopsies showed that long-term use of ERT reduced Gb3 accumulation in podocytes but did not alter podocyte injury. A novel CRISPR-/CAS9-mediated -Galactosidase knockout podocyte cell line confirmed ERT-mediated reversal of Gb3 accumulation without resolution of lysosomal dysfunction. Transcriptomic-based connectivity mapping and SILAC-based quantitative proteomics identified alpha-synuclein (SNCA) accumulation as a key event mediating podocyte injury.

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2021-10-06 | GSE185226 | GEO

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